Abstract
Abstract The differentiation of T cells along different lineages is central to the control of immunity. In order to investigate the role of PKCλ/ι, a member of atypical protein kinase C, in T cell function, we used a conditional gene knockout system by loxP-Cre recombination to selectively delete PKCλ/ι in activated T cells. With this system, we found that PKCλ/ι was necessary for Th2 cytokine production. Upon anti-CD3 plus anti-CD28 stimulation, IL-4 and IL-13 production from CD4+ T cells was significantly reduced in conditional KO mice as compared to their WT littermates. However, PKCλ/ι was not involved in Th1 cytokine secretion. T cell proliferation was impaired in conditional PKCλ/ι KO mice. Furthermore, deficiency of PKCλ/ι inhibited OVA-induced allergic airway inflammation in vivo. Our data demonstrated that the activation of the transcription factors NFAT and NF-¿B was impaired in PKCλ/ι-deficient activated T cells. In addition, we presented genetic knockout evidence in ex vivo experiments with primary T cells that PKCλ/ι was critical for the control of cell polarity during T cell activation. Therefore, PKCλ/ι emerges as a critical regulator of Th2 cell activation.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
